Bilateral Pulmonary Hyperaeration

Pulmonary Interstitial Emphysema

Figure 1.128. Bilateral pulmonary interstitial emphysema in another infant in which the radiograph shows the typical findings of hyperinflation and diffuse hyperlucencies within the lung parenchyma. This complication of hyaline membrane disease occurs most commonly as a complication of mechanically assisted ventilation and rarely occurs spontaneously. There is widespread rupture of alveoli resulting in accumulation of air in the interstitial lung tissue.

Figure 1.128. Bilateral pulmonary interstitial emphysema in another infant in which the radiograph shows the typical findings of hyperinflation and diffuse hyperlucencies within the lung parenchyma. This complication of hyaline membrane disease occurs most commonly as a complication of mechanically assisted ventilation and rarely occurs spontaneously. There is widespread rupture of alveoli resulting in accumulation of air in the interstitial lung tissue.

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Diffuse Emphysema Infant

Figure 1.129. The radiograph on the left shows severe hyaline membrane disease in the left lung and pulmonary interstitial emphysema in the right lung. This is an example of unilateral PIE in an infant with hyaline membrane disease. Within 24 hours, the hyaline membrane disease is resolving, as is the PIE. On chest radiograph, the irregular linear streakiness of pulmonary interstitial emphysema is typical of air dissecting into the large interstitial spaces of the lung.

Figure 1.130. In more severe cases of pulmonary interstitial emphysema, air can accumulate in the interstitium to the extent that it causes herniation of an involved lung across the midline. The incidence of severe interstitial emphysema has significantly decreased with widespread use of exogenous surfactant replacement.

Exogenous Pulmonary Surfactant Treatment

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Figure 1.131. In pulmonary interstitial emphysema, the complications of pneumothorax and pneumomediastinum are not uncommon, with the result that air may extend into the pleural spaces, mediastinal space, pericardial space and even dissect down tissue planes into the abdominal cavity. Note the pulmonary interstitial emphysema, pneumomediastinum, and pneumoperitoneum.

Figure 1.132. Radiograph of the same infant as in Figure 1.131 2 hours later showing the pulmonary interstitial emphysema on the left side and a large pneumothorax on the right side with collapse of the lung and the continued presence of the pneumomediastinum and pneumoperitoneum.

Pneumomediastinum Treatment Newborn

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Massive Pneumoperitoneum

Figure 1.133. This radiograph of the chest shows massive bilateral pneumothoraces after resuscitative efforts. Note that these are both severe tension pneumothoraces in that both lungs have collapsed and both sides of the diaphragm are concave. In general, if the pneumothorax is not severe, there will be no concavity of the diaphragm. (Singleton, E., Wagner, M.)

Diaphragm Disorders

Figure 1.134. A gross specimen of the lung shows the severe extent of the pulmonary interstitial emphysema. Note that the upper lobe of the lung appears more affected.

Bulge Diphram
Figure 1.135. Histopathology of the lung shows the massively dilated, air-filled interstitial spaces and markedly thickened alveolar sacs in pulmonary interstitial emphysema.

Figure 1.136. Clinical findings suggesting the diagnosis of pneumothorax include increasing respiratory distress, a unilateral chest bulge, diminished breath sounds on the affected side, and especially restlessness or irritability. If there is a large tension pneumothorax, there is decreased cardiac output and an elevated central venous pressure with profound circulatory collapse. In this radiograph there is a large left tension pneumothorax pushing the mediastinum and heart to the right. Note the marked depression of the diaphragm.

Figure 1.137. The diagnosis of pneumothorax can be rapidly established by the use of a bright light source for transillumination, especially in premature infants. This approach results in prompt recognition of the pneumothorax and can quickly direct appropriate therapy. In this figure, note the outline of the chest wall with the electrode attached and the total collapse of the right lung. Pneumothorax may occur spontaneously in infants who did not receive resuscitative measures or, more commonly, as a complication of assisted ventilation of preterm infants. A large tension pneumothorax should be promptly evacuated with a thoracostomy tube. A small pneumothorax, especially in the absence of symptoms, does not require treatment.

Transillumination PneumothoraxTransillumination Pneumothorax

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Figure 1.138. A radiograph of this infant with severe hyaline membrane disease shows the complications of positive pressure ventilation. There is a large right tension pneumothorax, pneumomediastinum, and subcutaneous air in the neck. Note that although there is collapse of lung with a severe pneumothorax, total collapse has not occurred because of the poor compliance of the lung. If the pneumothorax is associated with a positive pressure air leak, there is rapid clinical deterioration with mediastinal shift and collapse of the lungs. Placement of a thoracostomy tube results in rapid clinical improvement.

Pulmonary Hyperaeration

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Pneumothoraces
Figure 1.139. This radiograph shows bilateral pneumothoraces with accumulation of air on both the medial and lateral sides of the lung in an infant lying supine. Again, note that the lungs are not completely collapsed because of the severe degree of lung disease.

Figure 1.140. Air dissecting into the thorax and mediastinum may elevate the lobes of the thymus, resulting in the "butterfly wing" appearance of the lobes of the thymus gland. Clinically, pneumomediastinum is usually asymptomatic but findings may include a sternal bulge, restlessness or irritability, tachypnea, and distant heart sounds. Hamman's sign (a crunchy sound synchronous with the heart beat) is rarely present in the newborn period. Rupture of alveoli into the mediastinal space with accumulation of air around the heart does not usually require active management, except in extreme cases. (Singleton, E., Wagner, M.)

Figure 1.141. A lateral chest radiograph of the same infant as in Figure 1.140 shows air in the anterior mediastinum behind the sternum with elevation of the thymus. Note the well-outlined thymus gland and the subcutaneous air in the neck. (Singleton, E., Wagner, M.)

Figure 1.142. In this pathologic specimen note the multiple blebs dissecting through the soft tissue planes of the mediastinum as a result of a pneumomediastinum.

Spontaneous Pneumothorax Blebs

Figure 1.143. A rare complication associated with a pneumomediastinum is a subpleural collection of air. The air tracks between the parietal pleura and the diaphragm as seen in die anteroposterior and lateral radiographs of this infant.

Figure 1.143. A rare complication associated with a pneumomediastinum is a subpleural collection of air. The air tracks between the parietal pleura and the diaphragm as seen in die anteroposterior and lateral radiographs of this infant.

Diaphragm Disorders

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Figure 1.144. The chest radiograph of this infant shows a right pneumothorax and a pneumomediastinum. Note the lobes of the thymus gland displaced superiorly by the pneumomediastinum giving the "butterfly wing" appearance.

Figure 1.144. The chest radiograph of this infant shows a right pneumothorax and a pneumomediastinum. Note the lobes of the thymus gland displaced superiorly by the pneumomediastinum giving the "butterfly wing" appearance.

Bilateral Pneumothorax Images

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Thymus Gland Disorders

Figure 1.145. Three hours after the radiograph in Figure 1.144 was taken, the infant's condition had deteriorated and a repeat radiograph showed progression of the airblock widi the development of a pneumopericardium. Clinically there is sudden deterioration with a marked decrease in peripheral circulation, marked decrease in blood and pulse pressure, and an elevated central venous pressure.

Figure 1.146. Pneumopericardium is a rare, but potentially fatal, form of airblock with accumulation of air around the heart. There are distant or absent heart sounds. Rupture of alveoli leads to interstitial emphysema and tracking of air along the pulmonary veins into die pericardial sac. This may resolve spontaneously or may result in cardiac tamponade with muffled heart sounds and poor cardiac output. The pericardium is readily seen as a line of increased density between the air surrounding the heart and the air infiltrating the lung.

Figure 1.147. This infant on positive pressure ventilation developed a pneumothorax, pneumomediastinum, massive pneumopericardium, and subcutaneous emphysema in the neck, and especially on the left side of the chest. A massive pneumopericardium such as this always results in cardiac tamponade. Subcutaneous emphysema can be recognized clinically by crepitant bulging in the neck or over the chest, and results from the dissection of air from a pneumomedi-astinum. See Figure 7.71 in Volume I, Chapter 7.

Figure 1.148. Poor lung compliance with hyaline membrane disease and positive pressure ventilation can lead to the development of severe air leaks. In this instance, air has dissected into the mediastinum, the abdominal cavity, and the subcutaneous tissue. In the lateral radiograph, the pneumomedi-astinum outlines the thymus gland. The air in the peritoneal cavity must be distinguished from that of a ruptured viscus. Thoracic air can dissect through any or all of the diaphragmatic apertures: the vena cava, aorta or esophagus. Especially on the lateral radiograph, note the large amount of subcutaneous air.

Figure 1.149. Extensive air leaks occurred in this male infant on positive pressure ventilation. Note the subcutaneous air over the scalp, chest and abdominal walls, and in the scrotum. In pneumoperitoneum associated with tracking down of air from a pneumomediastinum, no air/fluid levels are seen in the abdomen. With pneumoperitoneum associated with a perforation, air/fluid levels are present. In a pneumoperitoneum, air enters the scrotum via the patent processus vaginalis.

Wilson Mikity Syndrome

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Figure 1.150. In the most severe cases, air can dissect into the intravascular spaces. In this radiograph, note that the air has dissected into the venous system causing massive air embolism to the heart. Note that the portal venous system is also filled with air.

Air Embolism Newborn

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Trastronos Metabolicos

Figure 1.151. Massive air embolism occurs as a result of air dissecting into the vascular system and accumulating in the heart displacing blood. In this infant, note the air in the chambers of the heart and along the vessels in the neck and arms. Sudden fatal extravasation of gas into the circulatory system may occur apparently due to rupture of pulmonary veins in conjunction with high intra-alveolar pressures from positive pressure ventilation.

Figure 1.152. This is another example of a massive air embolism showing air dissecting into the vascular system. Note the air not only in the heart but also in the major vessels as clearly seen in the lateral radiograph.

Figure 1.153. A skull radiograph of the same infant as in Figure 1.152 shows a pneumoencephalogram produced by the massive air embolism introducing air into the ventricular system. There was an associated intraventricular hemorrhage.

Figure 1.154. Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease which occurs in infants who receive prolonged exposure to oxygen with positive pressure ventilation. There are four radiologic stages. Stage I occurs from 1 to 3 days of age and is indistinguishable from severe hyaline membrane disease. Stage II occurs between 4 to 10 days of age when the lungs become homogeneously opacified. Stage III occurs between 10 to 30 days of age when multiple small rounded areas of radiolucency appear as a result of focal alveolar emphysema somewhat similar to the "bubbly" appearance of the lung in Wilson-Mikity syndrome. Stage IV occurs after 30 days of age when the cystic areas of the lung coalesce into larger cysts particularly in the upper lobes, and streaky, linear areas of scarring appear.

Stage Four Bronchopulmonary Dysplasia

Figure 1.155. This chest radiograph of an infant with Stage IV BPD demonstrates pneumatocele formation in the left chest, prominent interstitial markings, and pulmonary edema. The circular hyperlucency seen over the mediastinum and right chest is an artifact caused by the hole in the incubator when the radiograph is taken from above.

Figure 1.156. Twenty-four hours later, the same infant as in Figure 1.155 had an increase in the cystic areas and the pneumatocele on the left was larger.

Figure 1.155. This chest radiograph of an infant with Stage IV BPD demonstrates pneumatocele formation in the left chest, prominent interstitial markings, and pulmonary edema. The circular hyperlucency seen over the mediastinum and right chest is an artifact caused by the hole in the incubator when the radiograph is taken from above.

Artifact Radiography

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Pulmonary Hyperaeration Left

Figure 1.157. A radiograph of die chest of the same infant as in Figure 1.155 and 1.156 5 days later shows progression to the chronic changes of scarring and pulmonary edema. Lung injury this severe is often complicated by cor pulmonale. The overall prognosis for these infants is that approximately one-third recover, one-third develop chronic respiratory disease, and one-third die of respiratory failure.

Figure 1.157. A radiograph of die chest of the same infant as in Figure 1.155 and 1.156 5 days later shows progression to the chronic changes of scarring and pulmonary edema. Lung injury this severe is often complicated by cor pulmonale. The overall prognosis for these infants is that approximately one-third recover, one-third develop chronic respiratory disease, and one-third die of respiratory failure.

Figure 1.158. Wilson-Mikity syndrome (pulmonary dysmaturity, "bubbly" lung syndrome) shares many of the same radiologic features as Stage III BPD but there is no history of preceding hyaline membrane disease or of excessive oxygen therapy. The lungs are somewhat hyperinflated and there is a prominence of interstitial markings. Wilson-Mikity syndrome is not currently recognized as a disease entity.

Figure 1.159. In an enlarged radiograph of lung markings at the costophrenic angle in the same infant as in Figure 1.158, the "bubbly" appearance of the lungs is noted. These radiographic features are usually pathog-nomonic in that they show diffuse linear and reticular areas of density within which are multiple cyst-like areas of hyperaeration.

Figure 1.160. Wilson-Mikity syndrome is often confused with BPD because of the similar appearance on chest x-ray. This syndrome typically begins with no sign of respiratory distress. Clinical evidence of respiratory distress may occur in the first few days of life, especially in premature infants. However, the syndrome may not become evident until several weeks after birth, with the onset of respiratory distress which is usually not as severe as is seen in hyaline membrane disease. Oxygen requirements are usually not high.

Hyaline Membrane Disease Ray Chest

Figure 1.161. This chest radiograph in the same infant as in Figure 1.160 at the age of 3 months demonstrates persistent hyperinflation and prominent lung markings. The infant gradually improved over a period of 6 months and oxygen requirements were minimal.

Figure 1.162. This infant was normal at birth, but at 1 week of age developed severe dehydration with cardiovascular symptoms and a severe metabolic acidosis. The chest radiograph on die left shows die markedly hyperinflated lungs with a small cardiac silhouette. The diagnosis of a salt-losing congenital adrenal hyperplasia was established. There was rapid improvement following rehydration and base administration, as noted in the chest radiograph on the right taken 2 hours later in which die lung fields and heart size appear normal. Severe dehydration associated with gastroenteritis can result in a similar problem.

Figure 1.162. This infant was normal at birth, but at 1 week of age developed severe dehydration with cardiovascular symptoms and a severe metabolic acidosis. The chest radiograph on die left shows die markedly hyperinflated lungs with a small cardiac silhouette. The diagnosis of a salt-losing congenital adrenal hyperplasia was established. There was rapid improvement following rehydration and base administration, as noted in the chest radiograph on the right taken 2 hours later in which die lung fields and heart size appear normal. Severe dehydration associated with gastroenteritis can result in a similar problem.

Hyperinflation Lungs Infants

Figure 1.161. This chest radiograph in the same infant as in Figure 1.160 at the age of 3 months demonstrates persistent hyperinflation and prominent lung markings. The infant gradually improved over a period of 6 months and oxygen requirements were minimal.

Scaphoid Abdomen Infants
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Responses

  • Selina Galbassi
    What is a bilateral pulmunary hyperaeration?
    6 years ago
  • Pamela Lirette
    What is bilateral pulmonary emphysema?
    6 years ago
  • katja
    What is bilateral pulmonary hyperaeration?
    6 years ago
  • William
    When lungs hyperaerated bilaterally?
    5 years ago
  • Malva
    What is hyperaration in infants?
    4 years ago
  • roddy christie
    What is hyperaeration bilaterally?
    4 years ago
  • eyob
    What is bilateral pulmonary hyperinflation?
    2 years ago

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